The ability to stimulate or exercise muscle tissue is critical to the development and rehabilitation of muscle. In nature, alterations in ion channels cause the brain to generate electronic impulses or synapses. An impulse propagates along an axon to its termination on its way to initiating a muscle contraction. As such, characteristics of the impulse complement the active processes of the nervous system. Mechanically generated attempts to stimulate muscles often strive to emulate natural impulses, working within the confines of axon receptors. Therapists and athletes use machines that produce variations of such signals to develop muscle tissue by inducing a series of contractile twitches that aggregate to form a contraction. Benefits of such stimulation include the promotion of blood flow and the localized development of muscle tissue.
Conventionally, such signals embody a series of discontinuous pulses. Despite charges being measurable in millivolts, each pulse communicates at least a minimum threshold potential to a muscle. A threshold potential corresponds to a voltage level, or charge, as measured at a motor nerve, where the membrane of an axon experiences depolarization. Also called a firing level, it coincides with the moment of a twitch, where the potential in the axon releases its energy into a calcium/adenosine triphosphate (ATP) union at one or more toggling bridges in the sarcomere until the axon arrives at zero potential.
In this manner, the threshold potential presented via each pulse initiates a full-fledged twitching reaction. That is, sarcomere tissue of a muscle creates one twitch worth of contractile force in response to an application of a generated threshold potential. Successive bridging of adjacent sarcomere tissue comprises a contraction. Of note, a toggling reaction will not occur if the stimulus is sub-threshold in magnitude, i.e., it fails to convey the requisite threshold potential. The contractile reaction at each bridge in the sarcomere is therefore all-or-none. In this manner, conventional techniques repeat pulses of identical potential and duration to produce consecutive twitches that add up to a contraction. In this manner, each pulse of a signal will theoretically stimulate a next twitch.
In nature, sarcomere bridges toggle simultaneously across the length of each muscle as individual twitches aggregate to form a single contraction. In this manner, the twitches are said to toggle uniformly across a muscle. Such uniformity evades electrical attempts to stimulate muscle. In contrast, conventional applications use single short pulses that may succeed in toggling a high concentration of sarcomere bridges near the electrodes, but ultimately fail to stimulate more distant bridges. That is, while a high frequency application may initially toggle more bridges, the shorter spacing of the pulses is too small to allow time for depolarization and nutritional replenishment, ultimately frustrating continuing contraction.
As such, any contractile reaction initiated by the pulse is ended within a fraction of a second. Conversely, if the pulse rate is made slow enough to allow for depolarization and nutritional replenishment, accommodation drops in proportion to the drop in frequency, thus the deeper penetration is made possible. However, penetration comes at the expense of pain from the yanking and dropping effect produced by the toggling, de-toggling, re-toggling of more and more bridges in more sarcomeres with the increase in time between pulses as the frequency drops.
Other prior art techniques attempt to affect larger portions of the muscle by extending pulse length. However, such attempts still fail to achieve a uniform contraction. Namely, sarcomere bridges of the portion of the muscle nearest to the electrodes will release due to polarization and nutritional problems prior to an adjacent portion of the muscle toggling. The duration of the pulse causes the bridges in sarcomeres closer to the center of the muscle to toggle, but only at the cost of painfully yanking the spent and relaxing sarcomeres nearest the electrodes into a stretched condition as the process travels in a wave or ripple effect outward from the electrodes, but inward toward each other.
By the time the bridges in the middle sarcomeres begin to toggle, the mass of the muscle has developed a crushing velocity to add to the twitch. Those sarcomeres of the muscle nearest the electrodes have already been spent. Despite the relatively weaker twitch of the center sarcomeres, the hyper-compression, as the sum of the above, nonetheless, tugs on adjacent sarcomeres. Over time, repeated applications will increasingly stress and deplete energy supplies of muscle tissues. Repeated applications further produce relatively little beneficial effect, because the muscles are being stretched out of shape, traumatized almost as much as they are being treated. Additionally, high currents associated with long pulses stings the skin of the user. Thus, stimulation of sarcomeres distally positioned from the electrodes has not been possible without incurring preclusive pain and potential damage.
Known techniques used to address such factors include incorporating periods of recovery in between pulses. Sufficient lengths of such periods may allow the muscle to partially prepare for another contractile twitch. Muscle may use this short period between pulses to replenish a portion of expended ATP and calcium ions before the contraction process continues, re-initiated by a subsequent pulse. Each rest time between pulses also allows the body an opportunity to partially reset electrical polarities skewed by its preceding pulse by dissipating capacitance retained in the skin.
Despite these provisions, known pulse applications still suffer diminished returns with successive pulses due to nutritional depletion and motor-nerve boredom. Unless the pulse rate is so slow that it causes a painful, jerking sensation, there is inadequate time between pulses to allow for complete replenishment and electrical recovery. Consequently, pulses of repeated strength and duration incrementally drain overall muscle resources. As the muscles strength and supply wane, so does the muscle's ability to contract. As such, a subsequent pulse, identical in polarity, amplitude, shape and timing produces shallow contractions that result in less penetration than the preceding pulse. Less penetration translates into less muscle development, as weaker contractions fail to increase blood flow to required muscle tissue levels as needed for muscle development.
Still other obstacles hinder the effectiveness of conventional pulse signal applications. Namely, accommodation may prevent repeated pulses from penetrating deeply into the muscle, mitigating the potential benefit of successive pulses. Muscle accommodation regards the ability of the body to adapt to constant and repeated stimuli. Such stimuli includes the successive pulses of conventional muscle stimulators. As such, a muscle adapts to subsequent pulses in such a manner as it fails to achieve the same level of potential in response to a repeated pulse. Two major factors contributing to accommodation relate to electrical polarity and nutritional supply as discussed herein.
To compensate for the detrimental effects of accommodation, some applications attempt to increase the voltage of subsequent pulses to maintain comparable levels of stimulation. Other applications attempt to combat accommodation by varying pulse shape, width, height and frequency. Although such techniques can realize somewhat greater contractile reactions with less voltage, a targeted muscle still twitches in response to each pulse to a lesser degree than to the previous pulse. Further, while marginally effective in temporarily achieving deeper penetration, such attempts still result in preclusive pain that frustrates further treatment. In part, this pain stems from inability of known application and pulse variations to affect motor nerves (associated with muscle development) to the same degree as sensory nerves (associated with pain). In this manner, conventional pulse designers are limited in the range of voltage they can apply and the depth of contractile reactions they can achieve.
Significantly, conventional techniques further fail to uniformly address different types of muscle implicated in a treatment/development session. An inability of prior art pulse applications to simultaneously and consistently stimulate both slow and fast twitch muscle types often results in disproportionate muscle development. Such undesirable development detrimentally impacts balance, mobility and other motor considerations. The absence of uniformity is, in part, a product of how a single pulse induces different reactions in dissimilar muscle types of a user. For instance, as a signal propagates through a patient or athlete, fast and slow twitch muscles respond differently to conventional pulses. This limitation is a product of the different sensitivities and reaction rates of slow and fast twitch muscles.
Fast twitch muscle is developed in response to frequent, quick use. Fast twitch muscle is common in muscle groups that control fine motor functions, such as the wrist and hand. Consequently, fast twitch muscles process electrical stimuli relatively quickly. Of note, such muscles are prone to tire quickly and are vulnerable to overstimulation, causing tetany, a painful tightening of muscles. In contrast, slow twitch muscles react more slowly to stimuli than do fast twitch muscles, and they tire less easily. Slow twitch muscles are developed where smooth, methodical muscle contractions are common. For instance, regular motions and support realized by muscles of the back will typically develop associated muscles as slow twitch.
The disparate reactive characteristics of slow and fast twitch muscles preclude known transcutaneous signals from uniformly addressing both muscle types. Namely, no conventional pulse train can simultaneously sustain even distribution of contractile twitching reactions throughout both fast and slow twitch muscles. More particularly, a conventional train of pulses having a frequency synchronized with the response time of a fast twitch muscle is too quick for a slow twitch muscle to react to its fullest extent for the voltage applied.
Such an application, to a great degree, fails to stimulate slow twitch muscles and almost exclusively activates fast twitch muscles because the signal fails to propagate profound contractile twitches within the sarcomere of the slow twitch muscle. That is, the signal neglects the slow twitch muscle in favor of the fast twitch when both are inline with a signal, resulting in disproportionate development. Of note, high frequency pulses may still cause overstimulation in the fast twitch muscle. Such over-stimulation causes fast twitch muscles to painfully tighten, ending a therapeutic session before any gain can be realized in the slow twitch muscle.
Conversely, slowing the frequency of pulses so as to target slow twitch muscles can produce dissatisfactory results in fast twitch muscles. Thus, any gains realized in the slow twitch muscle group may be tempered by ineffectual and painful reactions in proximate fast twitch muscles. For instance, slow pulse rates may promote a painful, jerking reaction in fast twitch muscles. As a result, the rate of consecutive pulses may be too infrequent or painfully preclusive to substantially exercise or tax fast twitch muscles relative to the slow twitch muscle. In this manner, fast twitch muscles can act as a barrier to treatment of slow twitch muscles in that the high sensitivity and low pain threshold of the fast twitch muscles precludes more extensive propagation of twitches throughout slower twitch muscles. As such, exercising slow twitch muscles remains a challenge to conventional stimulators.
Consequently, what is needed is a single signal capable of uniformly exercising muscle tissue, while accounting for nutritional, comfort and accommodation considerations.